ライフサイエンスコーパス: HRG

1 HRG also promotes HA- and CD44-dependent oncogenic event

2 HRG bound specifically to apoptotic Jurkat cells and mat

3 HRG caused prominent induction in the nuclear expression

4 HRG caused the phosphorylation of serine 167 in ERalpha.

5 HRG decreased the dose required for BP-mediated stimulat

6 HRG deficiency was associated with a suppressed antitumo

7 HRG expression levels define a biologically distinct sub

8 HRG has antibacterial activity, and when challenged by H

9 HRG induces tumorigenicity and metastasis of breast canc

10 HRG loss influences macrophage gene regulation, leading

11 HRG mitogenic activity was also impaired by depletion of

12 HRG regulated the association of Ebp1 with E2F promoter

13 HRG siRNA inhibited growth of H1047R but not E545K-expre

14 HRG stimulation increased the homodimeric fraction of Er

15 HRG stimulation of cells co-expressing ErbB3 and ErbB2 l

16 HRG treatment induced a transient phosphorylation of BRC

17 HRG treatment led to degradation of poly (ADP-ribose) po

18 HRG, administered as a single dose, is reasonably well t

19 HRG-1 and HRG-4 are previously unknown transmembrane pro

20 HRG-2 is a type I membrane protein that binds heme and l

21 HRG-3 binds heme and is exclusively secreted by maternal

22 HRG-3 deficiency results either in death during embryoge

23 HRG-beta1 did not activate Akt in MCF-7 cells stably tra

24 HRG-induced Rac activation was phosphatidylinositol 3-ki

25 HRG/M was unable to autophosphorylate the erbB receptors

26 RNA that the growth factor heregulin beta 1 (HRG), a combinatorial ligand for human epidermal growth

27 olocalize within nuclei of heregulin beta 1 (HRG)-stimulated cells and both proteins bind to the endo

28 MCF-7/HRG cells were more than 10-fold resistant to the alkyla

29 itaxel or vincristine) was obtained in MCF-7/HRG cells.

30 ) engineered to overexpress heregulin (MCF-7/HRG), a ligand for the Her-2/3/4 network, we investigate

31 E(2)-induced Erk activation is mediated by a HRG/HER-2/PKC-delta/Ras pathway that could be crucial fo

32 In addition, HRG stimulation caused a significant decrease in BRCA1 m

33 In addition, HRG stimulation of breast cancer cells promoted phosphor

34 n, ATPase activity, and relocalization after HRG treatment could all be blocked by pretreatment with

35 lts suggest the potential use of Hst against HRG-mediated growth of breast cancers with high and low

36 Ebp1 could bind E2F consensus elements in an HRG-inducible manner, leading to transcriptional repress

37 It is thought that an HRG fragment containing the HRR, released via plasmin-me

38 HRG expression in MDA-MB-231 cells using an HRG antisense cDNA.

39 HRG-1 and HRG-4 are previously unknown transmembrane proteins, whi

40 (rs710446, combined p = 9.52 x 10(-22)), and HRG (rs9898, combined p = 1.34 x 10(-11)).

41 pleckstrin homology (PH) domain of Akt, and HRG-beta1 did not induce Akt phosphorylation in the ER-n

42 The combination of BP and HRG also stimulated proliferation of BT-474 cells compar

43 BP and HRG produced a synergistic increase in ERalpha recruitme

44 Butylparaben (BP) and HRG produced a synergistic increase in c-Myc mRNA and pr

45 abolished the formation of constitutive and HRG-induced ErbB3/ErbB2 heterodimers, it only slightly b

46 ndent BRCA1 phosphorylation and that ECM and HRG down-regulate BRCA1 expression in breast cancer cell

47 man breast cancer cells with CXCL12, EGF and HRG, and HMEC-CXCR2 cells with CXCL8 facilitated nuclear

48 esponse to stimulations with ligands EGF and HRG.

49 significantly lower than that of ErbB3, and HRG induced a less pronounced decrease in the diffusion

50 sized that ECM may affect the expression and HRG-dependent phosphorylation of BRCA1.

51 ression by siRNA reduced Slug expression and HRG-induced EMT.

52 11)In-bsRICs composed of trastuzumab Fab and HRG exhibited specific binding in vitro to tumor cells d

53 rt environmental heme into the intestine and HRG-3, a secreted protein, to deliver intestinal heme to

54 y was accelerated in HRG-deficient mice, and HRG administration abrogated this effect.

55 echanistic link between metabolic stress and HRG/TGZ-induced cell death.

56 Because HRG-mediated HAS isozyme phosphorylation/activation can

57 In breast cancer cells, heregulin beta1 (HRG) causes a strong activation of Rac; however, it does

58 nation with the HER4 ligand heregulin-beta1 (HRG) resulted in apoptosis of BT20 cells providing a nov

59 the HER3-binding peptide of heregulin-beta1 (HRG) with or without a 12- or 24 mer polyethylene glycol

60 Heregulin-beta1 (HRG), a combinatorial ligand for human epidermal growth

61 f MCF-7 cells with 10(-9) M heregulin-beta1 (HRG-beta1) resulted in a rapid phosphorylation of Akt an

62 rowth factor-I (IGF-I), and heregulin-beta1 (HRG-beta1), can modulate the expression and activity of

63 show that inhibitors of c-Src or HSP90 block HRG-induced targeting of MUC1 to mitochondria and integr

64 Although Hst blocked HRG signaling in both parental and HER-2 transfected cel

65 These studies were achieved by blocking HRG expression in MDA-MB-231 cells using an HRG antisens

66 ErbB4 was activated by both HRG-beta1 and HB-EGF stimulation; however, compared with

67 ssion strongly stimulated the levels of both HRG receptors.

68 Purified HRG protein induced, but HRG-deficient serum prevented, M1 macrophage differentia

69 tibacterial activity, and when challenged by HRG, sHIP was found to rescue S. pyogenes bacteria.

70 lerate AR mRNA decay was further enhanced by HRG treatment.

71 ere, we show that cellular import of heme by HRG-1-related proteins from worms and humans requires st

72 activity was also significantly increased by HRG treatment.

73 d Slug transcriptional activation induced by HRG or HSF-1 overexpression.

74 Although the invasion induced by HRG-beta1 or CXCL12 is dependent on the EGF/CSF-1 paracr

75 ensitization of the Rac response/motility by HRG are mediated by the transcription factor hypoxia-ind

76 Akt phosphorylation by HRG-beta1 was abrogated by an arginine to cysteine mutat

77 these cells restored Akt phosphorylation by HRG-beta1, suggesting the requirement of ER-alpha.

78 KCalpha attenuated the apoptosis produced by HRG and GF.

79 hed that, surprisingly, activation of Rac by HRG is mediated not only by ErbB3 and ErbB2 but also by

80 fied as developmental were down-regulated by HRG, whereas those involved in transport were up-regulat

81 rovides an explanation for its regulation by HRG, an ErbB3 ligand.

82 , a downstream effector of Ras signaling, by HRG, a growth factor with diverse functions in breast ca

83 the GADD153 promoter was also stimulated by HRG-inducible ATF-4 and activated HER2 but not wild-type

84 Following stimulation by HRG, a strong increase in [(3)H]thymidine incorporation

85 In human breast cancer cells, HRG induced G3BP mRNA and protein expression.

86 Consequently, HRG-induced apoptosis in SKBr3 cells appeared to involve

87 A, thereby confirming a role for HER4 in DAC/HRG-induced apoptosis.

88 We hypothesized that liver-derived HRG is a critical endogenous modulator of hepatic macrop

89 Liver-derived HRG, similar to alarmins, appears to be an endogenous mo

90 Among patients whose tumors had detectable HRG mRNA and low HER2 (n = 57 [38%] of 151 with availabl

91 Exploratory analyses suggest that detectable HRG and low HER2, biomarkers that link directly to the m

92 B-EGF promoted resurfacing greater than EGF, HRG, or controls.

93 er EPR or HB-EGF treatments compared to EGF, HRG, ErbB3 only, or empty vehicle.

94 ct activation profiles in response to either HRG or EGF, with obvious differences in both the intensi

95 Here we show that Caenorhabditis elegans HRG-3 is required for the delivery of maternal heme to d

96 e expression of Hst in MCF7 cells eliminated HRG signaling through both mitogen-activated protein kin

97 of classical PKC isoforms (Go6976) enhanced HRG-induced apoptosis, whereas the PKCdelta selective in

98 F) and Ro318425 (Ro), significantly enhanced HRG-induced apoptosis as determined by flow cytometric a

99 These findings suggest that ECM enhances HRG-dependent BRCA1 phosphorylation and that ECM and HRG

100 ning significant signals were located on F5, HRG, KNG1, F11, F12 and ABO and have been previously rep

101 bB3) is physically linked to ErbB2 following HRG stimulation.

102 ing an evolutionarily conserved function for HRG-1.

103 milar receptor requirements are observed for HRG-induced actin cytoskeleton reorganization and mitoge

104 lidate this finding and should preselect for HRG expression and focus on cancers with low HER2 levels

105 Our results establish a role for HRG-3 as an intercellular heme-trafficking protein.

106 A-induced thrombin generation in plasma from HRG-deficient and wild-type mice.

107 ombin generation was enhanced in plasma from HRG-deficient mice, and accelerated clotting was restore

108 of the antiangiogenic cleavage product from HRG.

109 Furthermore, HRG expression is higher in recurrent SCCHN compared to

110 Furthermore, HRG treatment resulted in G3BP translocation to the nucl

111 the expression of hypoxic responsive genes (HRG) PYRUVATE DECARBOXYLASE (VvPDC), ALCOHOL DEHYDROGENA

112 Although multiple heme-responsive genes (HRGs) have been characterized within the free-living nem

113 we showed that histidine-rich glycoprotein (HRG) binds FXIIa and attenuates its capacity to trigger

114 ith albumin and histidine-rich glycoprotein (HRG) in mouse and human plasma by size-exclusion chromat

115 Histidine-rich glycoprotein (HRG) is a 75-kDa heparin-binding plasma protein implicat

116 Histidine-rich glycoprotein (HRG) is a plasma protein consisting of 6 distinct functi

117 interacts with histidine-rich glycoprotein (HRG), and the name sHIP (streptococcal histidine-rich gl

118 plasma protein, histidine-rich glycoprotein (HRG), was demonstrated, in mouse tumor models, to mediat

119 at targeting prevention to high-risk groups (HRG) could be very effective.

120 titis significantly up-regulated hepatocytic HRG expression, which was associated with M1 polarizatio

121 Heregulin (HRG) is an activator of the erbB2-, erbB3- and erbB4-(er

122 Heregulin (HRG)-induced cell responses are mediated by the ErbB fam

123 HER-2 (erbB2) leads to amplified heregulin (HRG) signaling, promoting more aggressive breast cancer

124 creased with HER ligands, such as heregulin (HRG).

125 ng, the protein was identified as heregulin (HRG)alpha.

126 eceptor (HER) 3 (ErbB3), blocking heregulin (HRG) -mediated ErbB3 signaling and inducing ErbB3 recept

127 y an antibody against HER-2 or by heregulin (HRG) depletion from the conditioned medium through immun

128 e effects of ErbB-2 activation by heregulin (HRG) on BRCA1 function.

129 The growth factor heregulin (HRG), a ligand of ErbB3 and ErbB4 receptors, contributes

130 The growth factor heregulin (HRG), expressed in about 30% of breast cancer tumors, ac

131 The ErbB3/4 ligand heregulin (HRG) profoundly affects cell growth and differentiation,

132 es crosstalk between ErbB3 ligand heregulin (HRG)-triggered signaling and the AR axis, affecting biol

133 upregulated the HER3/HER4 ligand heregulin (HRG).

134 3) integrin and overexpression of Heregulin (HRG), a growth factor associated with breast cancer aggr

135 r cells exhibiting high levels of Heregulin (HRG), a growth factor closely associated with a metastat

136 epidermal growth factor (EGF) or heregulin (HRG) results in marked upregulation of MUC1-C translatio

137 epidermal growth factor (EGF) or heregulin (HRG), significantly improves prediction of cell migratio

138 with these results, we show that heregulin (HRG), a ligand for ErbB receptors, activates c-Src and,

139 We now show that heregulin (HRG), but not EGF, stimulates p95ErbB2 phosphorylation i

140 hese mechanisms, we observed that heregulin (HRG)-mediated activation of HER2, or HER2 overexpression

141 The heregulin (HRG) receptor, ErbB3, must heterodimerize with other mem

142 Addition of the ErbB-ligand, Heregulinbeta1 (HRG), to breast tumour-derived T47D cells promotes D-cyc

143 to quantify the contribution of heterosexual HRGs and the potential impact of focused interventions t

144 We show that high HRG expression is associated with activated HER3, wherea

145 (PE)HRG214 (HRG) is a polyclonal antibody preparation produced by im

146 Caenorhabditis elegans and human HRG-1-related proteins are conserved, membrane-bound per

147 w, by exploiting this auxotrophy to identify HRG-1 proteins in C. elegans, that these proteins are es

148 ctional blockade of alpha(v)beta(3) impaired HRG-promoted hyperactivation of ERK1/ERK2 MAPK without a

149 Taken together, our results implicate HRG-2 as a facilitator of heme utilization in the Caenor

150 In HRG-induced UBs, however, the expression of GFRalpha1 wa

151 Cytochrome heme profiles are aberrant in HRG-2-deficient worms, a phenotype that was partially su

152 lusion after FeCl3 injury was accelerated in HRG-deficient mice, and HRG administration abrogated thi

153 further evidence of a key role for CYR61 in HRG-dependent alpha(v)beta(3) overexpression.

154 Forced expression of CYR61 in HRG-negative MCF-7 cells notably upregulated the express

155 f Bcl-2 protein and further degraded PARP in HRG-treated cells.

156 dium-hydrogen exchanger2 was up-regulated in HRG-treated UBs compared with UBs grown in the presence

157 ivity, demonstrating a direct causal role in HRG induction of tumorigenicity.

158 oss after tail tip amputation was similar in HRG-deficient and wild-type mice, carotid artery occlusi

159 tic and proliferative cascades and inhibited HRG-induced Her-2/3 phosphorylation.

160 -activating protein beta2-chimerin inhibited HRG-induced ERK activation, mitogenicity, and migration

161 MDM, while DNA, but not chromatin, inhibited HRG binding to apoptotic cells, and either anti-FcgammaR

162 Anti-FcgammaRI mAb inhibited HRG binding to HMDM, while DNA, but not chromatin, inhib

163 The PI3K inhibitor BEZ235 markedly inhibited HRG and pAKT levels and, in combination with lapatinib,

164 ic small interfering RNAs) not only inhibits HRG-mediated HAS phosphorylation/activation and HA produ

165 Interestingly, HRG expression in tumor biopsies from invasive breast ca

166 In this study we have investigated HRG activation of ErbB2, extracellular signal-regulated

167 and VWF, with the leading variants in KNG1, HRG and F12 being the same as in the EAs; the significan

168 significant signals were identified in KNG1, HRG, F12, ABO and VWF, with the leading variants in KNG1

169 previously reported associations with KNG1, HRG and F12 in EAs.

170 previously reported associations with KNG1, HRG, F11, F12, and ABO were confirmed.

171 Transfection of full-length HRG cDNA into the estrogen (E2)-dependent cell line MCF-

172 re we explore the hypothesis that high-level HRG expression defines a subpopulation of SCCHNs with ac

173 ng to EGFR and HER3, suggest that high-level HRG expression was associated with clinical response in

174 MTLn3 cells in response to the ErbB3 ligand HRG-beta1.

175 Our findings suggest that Ebp1, by linking HRG activation of membrane receptors to E2F gene activit

176 associated with activated HER3, whereas low HRG expression is associated with low HER3 activation in

177 h of HRG-overexpressing cells, while the low-HRG-expressing 231/AS31 cells did not show a significant

178 ve shown that the heme transporter B. malayi HRG-1 (BmHRG-1) is indeed functional in B. malayi In add

179 ls were seeded on laminin (LAM) or Matrigel, HRG induced a significantly higher proliferation than it

180 ting a role of oxidative stress in mediating HRG/TGZ-induced cell death.

181 Therefore, in a nucleic acid-driven model, HRG inhibits thrombosis by modulating the intrinsic path

182 Moreover, HRG expression in MCF-7 cells renders the cells sensitiv

183 Moreover, HRG promoted growth of UBs cultured in the absence of GD

184 Moreover, HRG-deficient mice showed significantly enhanced hepatic

185 -7 cells overexpressing a structural mutated HRG isoform.

186 ding EGF (HB-EGF), and heregulin/neuregulin (HRG).

187 Notably, HRG treatment upregulates surface expression levels of C

188 Her-2 phosphorylation, the majority (67%) of HRG-overexpressing and Her-2 tumors (n = 57; 30%) were i

189 oph that requires the coordinated actions of HRG-1 heme permeases to transport environmental heme int

190 sociation of the tumor-promoting activity of HRG from the sensitization to Doxo, that is, although th

191 ture confirmed the proliferative activity of HRG.

192 We demonstrate that assessment of HRG expression and Her-2 activation define a particular

193 sion was noticeably decreased by blockade of HRG expression in the 231/ASPOOL, 231/AS31 and Hs578T/AS

194 -2 overexpression concludes that blockage of HRG expression suppresses the aggressive phenotype of MD

195 earch for the mechanism by which blockage of HRG reverts this aggressive phenotype, we discovered tha

196 Taken together, the combination of HRG and TGZ may provide a basis for the development of a

197 estion, while neutralization or depletion of HRG from sera reduced this effect.

198 the effects exerted by the downregulation of HRG expression as well as by functional blockade of alph

199 empt to dissociate the tumorigenic effect of HRG from the sensitizing effect to chemotherapy, we cons

200 as PI 3-K inhibitors, blocked the effect of HRG-beta1 on ER-alpha expression and activity and on the

201 bB inhibitors demonstrate that the effect of HRG-beta1 on ER-alpha expression and activity is also me

202 titutively active Akt mimicked the effect of HRG-beta1.

203 be a downstream modulator of the effects of HRG on cell cycle progression.

204 B2 is the primary mediator of the effects of HRG-beta1 on ER-alpha regulation.

205 The preadministration of an excess of HRG decreased uptake in MDA-MB-468 (HER2-negative/HER3-p

206 as HC, induce transiently the expression of HRG and VvFT and hasten the sprouting of endodormant gra

207 ation, induces transiently the expression of HRG and VvFT, and in the long-term, along with the advan

208 We propose that high-level expression of HRG is associated with constitutive activation of HER3 i

209 dimerization and high-level co-expression of HRG.

210 echanism underlying the diverse functions of HRG is not well established but is believed to depend on

211 in the modulation of uncontrolled growth of HRG-overexpressing breast carcinomas.

212 ility and anchorage-dependent cell growth of HRG-overexpressing cells, while the low-HRG-expressing 2

213 we examined whether CYR61, independently of HRG, actively regulates breast cancer cell survival and

214 To date, structural information of HRG has largely come from sequence analysis and spectros

215 SCCHN tumors express the highest levels of HRG compared to a diverse collection of other tumor type

216 Therefore, controlling tissue levels of HRG or PGF might be a promising strategy in chronic infl

217 cells expressing endogenously high levels of HRG.

218 tablished that Rac is a critical mediator of HRG mitogenic signaling in breast cancer cells and highl

219 treatment with LY294002 reduces migration of HRG-stimulated cells but not EGF-stimulated cells, despi

220 Transfection of the deletion mutant of HRG described in this study (HRG/M) into MCF-7 cells res

221 constructed a structural deletion mutant of HRG.

222 hich PKC isoform(s) mediated potentiation of HRG-induced apoptosis, the profile of PKC isoforms was m

223 c, cytoplasmic, and transmembrane regions of HRG-1-related proteins.

224 To investigate the role of HRG as a regulator of the intrinsic pathway, we compared

225 dominantly mediated through the secretion of HRG and activation of HER-2 by an autoctine/paracrine me

226 beta(3) in the proliferation and survival of HRG-overexpressing breast cancer models.

227 show that macrophages are a direct target of HRG.

228 RG-1, BmHRG-2, and BmMRP-5 (all orthologs of HRGs in C. elegans) are down-regulated in heme-treated B

229 n accordance, expression arrays conducted on HRG-treated peritoneal macrophages showed induction of g

230 invasion induced by EGF is not dependent on HRG-beta1 or CXCL12 signaling, showing an asymmetrical r

231 ssed in SKBr3 cells, the effect of Go6976 on HRG-induced apoptosis largely related to inhibition of P

232 tigate the impact of this HER-2 inhibitor on HRG-induced signaling, proliferation, and sensitivity to

233 s an important molecular interaction site on HRG, possesses a cystatin-like fold composed of a 5-stra

234 in competition assays with unlabeled Fab or HRG on cells expressing one or both receptors.

235 ut the preadministration of unlabeled Fab or HRG to determine the specificity of uptake.

236 Purified HRG or HRG in sera increased the number of HMDM-containing apop

237 of short gene lengths, multiple exons, other HRGs in B. malayi (BmHRG-3-6) remain unidentified.

238 reast cancer cells engineered to overexpress HRG, and significantly increased their sensitivity to Ta

239 heterologous plasma membrane heme permease (HRG-4), but the mode of suppression mediated by the Nce1

240 a isoform alone was sufficient to potentiate HRG-induced apoptosis.

241 rotein kinase and Akt pathways and prevented HRG-mediated proliferation.

242 tant, or small molecule inhibitors prevented HRG-induced HSF-1 activation and Slug expression.

243 was facilitated by the transmembrane protein HRG-2.

244 Purified HRG or HRG in sera increased the number of HMDM-containi

245 Purified HRG protein induced, but HRG-deficient serum prevented,

246 re of the N2 domain of serum-purified rabbit HRG.

247 The addition of recombinant HRG to the isolated UB grown in three-dimensional cultur

248 e trastuzumab coexposure completely reversed HRG-promoted CDDP resistance.

249 erapy efficacy in cells that did not secrete HRG, such as MCF-7 cells overexpressing a structural mut

250 ng alpha(v)beta(3) and its driven signaling, HRG blockade led to decreased levels of CYR61 in 231/ASP

251 etion mutant of HRG described in this study (HRG/M) into MCF-7 cells resulted in the dissociation of

252 In this phase I study, HRG was administered intravenously as a single dose (1,

253 ed Hst inhibited HER-3 levels and suppressed HRG-induced proliferation of MCF7 and BT474 breast cance

254 hat breast cancer cells exposed to sustained HRG treatment show markedly enhanced Rac1 activation and

255 rt and serves as a proof of the concept that HRG is a key promoter of breast cancer tumorigenicity an

256 To confirm that HRG modulates the contact system, we used DNase, RNase,

257 It was previously demonstrated that HRG induced the phosphorylation of BRCA1, which was medi

258 We demonstrated that HRG stimulation of mammary epithelial cells induces the

259 gether, these findings clearly indicate that HRG activation of ErbB2-ERK signaling modulates HAS phos

260 These results indicate that HRG is regulating alpha(v)beta(3) levels as well as alph

261 The findings indicate that HRG, by acting as a bridge between DNA on apoptotic cell

262 Assay of PKC activity indicated that HRG activated PKC in SKBr3 cells, predominantly affectin

263 In this study, we show that HRG potentiates the ingestion of apoptotic cells by matu

264 ta presented here paradoxically suggest that HRG expression can actually be beneficial when it comes

265 Taken together, the data suggest that HRG supports UB epithelial cell differentiation and non-

266 Taken together, our data suggest that HRG-beta1, bound to the ErbB2 ErbB3 heterodimer, in the

267 d either anti-FcgammaRI or DNA abrogated the HRG-dependent ingestion.

268 (O-t-butyl)-Ala-leucinal] inhibited also the HRG-induced down-regulation of BRCA1 protein in breast c

269 r, blockade of CYR61 expression impaired the HRG-induced hyperactivation of ERK1/ERK2 MAPK without al

270 a(5) and alpha(v)beta(6) was assessed in the HRG-overexpressing breast cancer cells MDA-MB-231, Hs578

271 oteosome inhibitor lactacystin inhibited the HRG-induced down-regulation of BRCA1 mRNA expression.

272 naling corresponded to downregulation of the HRG receptors, HER-3 and HER-4, whereas HER-2 overexpres

273 The activation of the HRG signaling axis has been considered as a poor prognos

274 fected with the antisense orientation of the HRG-beta2 full-length cDNA (231/ASPOOL, 231/AS31 and Hs5

275 Electron microscopic examination of the HRG-induced UB revealed the presence of structurally mat

276 EBP) homologous protein (CHOP) as one of the HRG-inducible genes.

277 Furthermore, our data indicate that the HRG-induced ErbB2.ErbB4 complexes stimulate ErbB2 tyrosi

278 Our data show that the HRG/M sequences are sufficient to sensitize MCF-7 cells

279 ecipitation of phospho-HER3, was compared to HRG expression in SCCHN samples.

280 Conjugation of Fab to HRG was confirmed by sodium dodecyl sulphate polyacrylam

281 ge function, indicating that invasiveness to HRG-beta1 is dependent on the EGF/CSF-1 paracrine loop.

282 hosphorylated wild-type BRCA1 in response to HRG in T47D cells, Cdk4 failed to phosphorylate the trun

283 orylation of p95ErbB2 and AKT in response to HRG was abrogated to varying degrees by GW572016.

284 m HCC-1937 cells was observed in response to HRG.

285 ot only was the elevated ErbB3 responsive to HRG-beta1-induced enhanced signaling mechanism, but also

286 TLn3-ErbB3 and transgenic MMTV-Neu tumors to HRG-beta1 is inhibited by blocking EGF receptor, CSF-1 r

287 able fraction (PAF) of HIV infections due to HRGs, or (b) the number per capita or fraction of HIV in

288 During the first 24 h after treatment, HRG and VvFT were strongly induced by hypoxia, subsequen

289 e combination of heregulin and troglitazone (HRG/TGZ) induced both apoptosis and necrosis, the main m

290 of BRCA1 and decreased BRCA1 expression upon HRG stimulation while overexpression of truncated BRCA1

291 was mediated through alpha(6) integrin upon HRG stimulation.

292 Our investigation into whether HRG is a factor likely to promote tumor formation indepe

293 e Her-2/3/4 network, we investigated whether HRG-induced transactivation of Her-2 affected breast can

294 otype, we discovered that the cells in which HRG is blocked exhibit a marked decrease in erbB activat

295 d HB-EGF stimulation; however, compared with HRG-beta1, HB-EGF induced phosphorylation of the 80-kDa

296 lerated clotting was restored to normal with HRG reconstitution.

297 ntrast, PS ASOs associate predominantly with HRG in monkey plasma because of higher concentrations of

298 BRCA1 in T47D cells 4 h after treatment with HRG compared to its level in control nontreated T47D cel

299 is-phenotypes that are fully rescued by worm HRG-1.

300 nt yeast strain, ectopically expressing worm HRG-2, revealed significantly improved growth at submicr